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Biomedical subjects

N B Ingels

Publications and source records attributed to N B Ingels.

88 records · Page 5Linked to original sources

Effects of relaxation therapy on cardiac performance and sympathetic activity in patients with organic heart disease.

Six patients, with surgically implanted tantalum myocardial markers, were trained in deep muscle relaxation therapy. Analysis of individual responses and group means of blood pressure and ventricular dimensions during relaxation showed a decrease in plasma norepinephrine levels and indices of myocardial contractility compared to the control state. Heart rate changes in individuals during relaxation were directly correlated with changes in plasma norepinephrine levels, although group means for heart rate did not change significantly between control and relaxation periods. Base-line plasma norepinephrine levels were directly correlated with systolic blood pressure and were inveresly correlated with a measure of myocardial contractility. These data suggest that physiological changes during relaxation may be mediated through the sympathetic nervous system.

Aged↗

Role of tachycardia as an inotropic stimulus in man.

We examined the inotropic effect of tachycardia in nine postsurgical aortocoronary bypass graft patients (with intact cardiac innervation) and nine cardiac allograft recipients (with denervated hearts). The changes in stroke volume (SV) and velocity of circumferential fiber shortening (VCF) which accompany sudden increases and decreases in atrial pacing frequency were determined by computer-aided fluoroscopic analysis of the motion of surgically implanted midwall myocardial markers. Because the first beat after a change in rate retains the frequency characteristics of the preceding rate, we compared the first posttachycardia beat with control beats and late tachycardia beats with the first tachycardia beat; afterload and preload for each pair of beats were similar. For an increase in heart rate of 50 beats/min, SV and VCF rose 79 and 64% from the first tachycardia beat to late tachycardia beats, and SV and VCF rose 8 and 35% from control beats to the first posttachycardia beat in the innervated group. Responses in the denervated group were not significantly different from those in the innervated group. The degree of the inotropic response was positively correlated with the magnitude of the increase in heart rate (r = 0.91). The decay in augmented contractility after decreasing the rate back to control levels fits an exponential relationship with a mean t((1/2)) of 1.7 s. Thus, in conscious man, increases in heart rate represent a positive inotropic stimulus, independent of other factors influencing ventricular performance and unaffected by neural innervation, and should be considered when changes in cardiac function are interpreted during serial studies or after drug administration.

Adolescent↗

Hemodynamic effects of intravenously administered quinidine on the transplanted human heart.

The acute hemodynamic effects of intravenously administered quinidine were studied in five heart transplant recipients with an anatomically denervated heart. Quinidine, 10 mg/kg body weight, was infused over a 20 minute period, and mild wall left ventricular dynamics were measured with a new technique using metallic markers surgically implanted in the myocardial wall. Heart rate was maintained constant with atrial pacing, and aortic blood pressure was measured through an indwelling catheter. In each patient the hemodynamic responses to quinidine were similar. End-diastolic, end-systolic and stroke volumes decreased by an average of 19, 26 and 18 percent, respectively. Cardiac output decreased by a mean 0.92 liters/min (-18%), and the mean aortic blood pressure decreased by 10 mm Hg (-11%). All of these changes were statistically significant. Three indexes of the contractile state of the left ventricle--mean circumferential velocity, mean systolic diameter shortening and ejection fraction--were not significantly changed. We conclude that quinidine exerts no acute inotropic myocardial effects in the human transplanted heart and that, when given intravenously, its hemodynamic action is most consistent with venodilatation.

Blood Pressure↗

Effects of heart rate augmentation on left ventricular volumes and cardiac output of the transplanted human heart.

The response of the donor left ventricle to atrial pacing was measured in 11 patients 12 to 64 days after cardiac transplantation. At operation seven miniature tantalum coils were placed into the midwall of the donor left ventricle so as to outline the ventricle in a 30 degrees right anterior oblique projection. Computer aided fluoroscopic analysis of marker dynamics allowed calculation of end-diastolic and end-systolic volumes, stroke volume, cardiac output, and ventricular filling characteristics. Recipients were studied in a resting, unsedated state during a period of clinical stability that did not immediately follow or precede an episode of graft rejection. Augmentation of heart rate by an average of 40 beats per minute above sinus rate produced significant reductions in end-diastolic volume (-19%), end-systolic volume (-8%), stroke volume (-31%), and the duration of systole (-19%), and diastole (-40%). Cardiac output was invariant with rate. In all patients, end-diastolic volume reduction at augmented rates was brought about by abbreviated diastolic filling as initiation of contraction occurred at an earlier point on a common, incremental filling curve. Previous studies have shown that the normal inverse relationship between heart rate and stroke volume is not available to the transplanted heart in the immediate postoperative period. The present study shows that this intrinsic mechanism becomes available to the denervated heart in the subsequent recovery period after surgery.

Cardiac Output↗

Measurement of midwall myocardial dynamics in intact man by radiography of surgically implanted markers.

Tiny radiopaque helices (0.85 times 1.5 mm) of pure tantalum wire were implanted by means of a simple insertor instrument into the left ventricular myocardium in 24 patients at the time of cardiac surgery. The markers were positioned in such a way as to outline the profile of the left ventricle when viewed in a 30 degree right anterior oblique projection. Biplane studies showed that all markers could be placed very nearly in a plane using the surface anatomy of the heart as a guide to implantation. Implantation of markers required approximately two minutes. No intraoperative or postoperative complications ascribable to the markers have occurred. They remain firmly in place and allow acquisition of a noninvasive ventriculogram at any time after surgery. The dynamic geometry of the left ventricle was determined by analysis of cineradiograms of these markers. Utilization of a single-plane (right anterior oblique) cineradiogram to obtain measurements of major transverse ventricular diameters, mean circumferential shortening, and circumferential shortening velocity results in underestimation of lenghts by 1.4%, overestimation of shortening by 1.2% of end-diastolic length, and overestimation of velocity by 0.05 circ/sec, when compared with values obtained simultaneously from biplane cineradiograms.

Cardiac Surgical Procedures↗

A biologically compatible implantable ultrasonic marker.

An implantable passive ultrasonic marker has been developed which can be detected with a conventional pulse echo imaging system. The marker consists of a planar array of 1/16 in. diameter stainless steel (316L) spheres and produces a distinct and characteristic reflection signature due to reverbation within the spheres. The marker has undergone both in vitro and in vivo tests and is biologically compatible for chronic implantation. It is consistently detectable at depths up to 10 cm from the transducer. An application to the detection of flow conditions in aortocoronary bypass grafts is suggested.

Animals↗

Pitfalls in creation of left atrial pressure-area relationships with automated border detection.

Creation of pressure-area relationships (loops) with automated border detection (ABD) involves correction for the variable inherent delay in the ABD signal relative to the pressure recording. This article summarizes (1) the results of in vitro experiments performed to define the range of, and factors that might influence, the ABD delay; (2) the difficulties encountered in evaluating a thin-walled structure like the left atrium in the dog model; and (3) the solutions to some of the difficulties found. The in vitro experiments showed that the ABD delay relative to high-fidelity pressure recordings ranges from 20 to 34 msec and 35 to 57 msec at echocardiographic frame rates of 60/sec and 33/sec, respectively. The delay was not influenced significantly by the type of transducer used, distance from the target area, or size of the target area. The delay in the ABD signal, relative to the echocardiographic image, ranges from nil to less than one frame duration, whereas it is delayed one to two frame durations relative to the electrocardiogram processed by the imaging system. In the dog model, inclusion of even small areas outside the left atrium rendered curves with apparent physiologic contour but inappropriately long delays of 90 to 130 msec. To exclude areas outside the left atrial cavity, time-gain compensation and lateral gain compensation were used much more extensively than during left ventricular ABD recording. By changing the type of sonomicrometers used in our experiments, we were able to record simultaneously ABD and ultrasonic crystal data. However, both spontaneous contrast originating from a right-sided heart bypass pump and electronic noise from the eletrocautery severely interferred with ABD recording.

Animals↗